Evidence map›Paper›PMID 37646156›Full record

ArticleCirculation research2023

SIRT3 Regulates Clearance of Apoptotic Cardiomyocytes by Deacetylating Frataxin.

Jing Gao, Chenglin Huang, Linghui Kong, Wugang Zhou, Mengwei Sun, Tong Wei, Weili Shen

Open access · hybridAbstract read
In one paragraph

Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 44 citations in OpenAlex.

  1. FXN predicts poor prognosis in colon adenocarcinoma and correlates with immune cell infiltration.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jing GaoDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital (J.G., C.H., L.K., T.W., W.S.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0009-0005-9071-7770
Chenglin HuangDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital (J.G., C.H., L.K., T.W., W.S.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0009-0005-7940-0297
Linghui KongDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital (J.G., C.H., L.K., T.W., W.S.), Shanghai Jiao Tong University School of Medicine, China.
Wugang ZhouDepartment of Emergency, Shanghai Ninth People's Hospital (W.Z.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0000-0001-8179-1083
Mengwei SunDepartment of Emergency, Shanghai Ninth People's Hospital (W.Z.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0000-0002-3394-1638
Tong WeiDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital (J.G., C.H., L.K., T.W., W.S.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0009-0003-4094-3468
Weili ShenDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital (J.G., C.H., L.K., T.W., W.S.), Shanghai Jiao Tong University School of Medicine, China.ORCID 0000-0002-3088-8245
Shanghai Institute of Hypertension · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEfferocytosis is an activity of macrophages that is pivotal for the resolution of inflammation in hypertension. The precise mechanism by which macrophages coordinate efferocytosis and internalize apoptotic cardiomyocytes remains unknown. The aim of this study was to determine whether SIRT3 (sirtuin-3) is required for both apoptotic cardiomyocyte engulfment and anti-inflammatory responses during efferocytosis.

methodsWe generated myeloid SIRT3 knockout mice and FXN (frataxin) knock-in mice carrying an acetylation-defective lysine to arginine K189R mutation (FXN

resultsWe showed that SIRT3 deficiency exacerbated Ang II-induced downregulation of the efferocytosis receptor MerTK (c-Mer tyrosine kinase) and proinflammatory cytokine production, accompanied by disrupted mitochondrial iron homeostasis in cardiac macrophages. Quantitative acetylome analysis revealed that SIRT3 deacetylated FXN at lysine 189. Ang II attenuated SIRT3 activity and enhanced the acetylation level of FXN

conclusionsThe SIRT3-FXN axis has the potential to resolve cardiac inflammation by increasing macrophage efferocytosis and anti-inflammatory activities.

Indexed as

Myocytes, CardiacSirtuin 3Animalsc-Mer Tyrosine KinaseFrataxinLysineMicec-Mer Tyrosine KinaseFrataxinLysineSirt3 protein, mouseSirtuin 3c-Mer tyrosine kinaseionsmacrophagesphenotypesirtuin 3

Identifiers

PMID37646156
PMCPMC10498872
OpenAlexW4386271668

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.